Cyclic Adenosine-3′,5′-Mconophosphate (cAMP for short) is a nucleotide Derivatives of it, it is an important substance that transmits nitrogen-containing hormones in the human body. When nitrogen-containing hormones are secreted from a certain cell and travel to the target cell with body fluids, they act on specific receptors on the cell membrane and activate adenosine cyclase in the cell membrane. This enzyme activates adenosine cyclase in the presence of Mg2+ or washed kaolin Ca2+. It converts adenosine triphosphate (ATP) in cells into cAMP, which then activates protein kinases. The protein kinases then activate various enzyme systems to exert powerful physiological effects. Therefore, nitrogen-containing hormones are called the first messenger and cAMP is the second messenger.
cAMP widely exists in various cells and plays an important regulatory role in cell function and metabolism. Pharmacological tests have shown that exogenous cAMP has the functions of relaxing smooth muscles, dilating blood vessels, improving liver function, promoting nerve regeneration, inhibiting cell division in the outer layer of skin and transforming abnormal cells. It can promote the activity of respiratory chain oxidases, improve myocardial hypoxia, etc. . A review of the clinical applications of exogenous cyclic adenosine monophosphate in recent years is as follows:
- Treatment of cardiovascular disease
Cyclic adenosine monophosphate (cAMP) is a nucleotide derivative that is involved in regulating substance metabolism in cells. It is an important substance for biological functions and has the functions of nourishing myocardium, inotropic force, potassium hydroxide relaxing blood vessels, and anti-arrhythmia. As the second messenger for the transmission of life information, cAMP can release Ca2+ from the ATP-Ca2+ complex on the cell membrane to change the function of the cell membrane; it can also cause Ca2+ in the sarcoplasmic reticulum to enter the muscle fiber, thereby enhancing myocardial contractility and increasing cardiac activity. discharge, and dilate the coronary arteries. Clinical observations show that exogenous cyclic adenosine monophosphate (cAMP) entering the body can directly or indirectly activate a series of protein kinases, increase the role of phosphorylase, and decompose glycogen to supply energy during hypoxia, thereby promoting oxidation of the respiratory chain. Activation of enzymes to improve myocardial hypoxia; inhibit the production of free radicals to prevent ischemia-reperfusion injury; increase the concentration of cAMP in the blood, thereby reducing the inflammatory response after ischemia and improving capillary permeability changes caused by ischemia .
Treating Hyperthyroidism
Patients with hyperthyroidism have obvious palpitation symptoms due to myocardial hypoxia, and because thyroid hormone stimulates the TRB receptors in the myocardium, leading to accelerated heart rate and tachycardia, it also stimulates the Na-K-ATPase in the cell membrane, consuming a large amount of ATP, thereby promoting mitochondrial The oxidative phosphorylation reaction leads to increased oxygen consumption and heat production, resulting in fatigue symptoms. Wang Lei et al. [9] administered cAMP 120 mg intravenously daily to 172 patients with hyperthyroidism. After 14 days, the symptoms of palpitation and fatigue in the cAMP treatment group were significantly improved. Cyclic adenosine monophosphate can increase the concentration of cytoplasmic calcium ions and improve the hypoxic state of cells. This may be the main reason why cyclic adenosine monophosphate improves symptoms of fatigue and palpitation. Since cyclic adenosine monophosphate does not affect the effect of thyroid hormone on TRβ, it has little effect on tachycardia. Similarly, since cAMP has no effect on the synthesis and release of thyroid hormones, it does not affect the recovery speed of TSH, FT3, and FT4.
- Treat neurological diseases
As one of the most important intracellular messengers, cyclic adenosine monophosphate plays a role in various biological processes in the body through cell signaling. Chemical reactions include playing an important role in wound repair. Studies have reported that cyclic adenosine monophosphate can promote the growth of neuronal processes, and the intracellular level of cyclic adenosine monophosphate in neurons is closely related to the neuronal process growth ability [3]. Through observation in rat spinal cord injury repair experiments, in vivo administration of cAMP can induce nerve regeneration after spinal cord injury in rats. Injection into the motor cortex of the brain and local spinal cord injury can induce significant spinal cord axon regeneration. Continuous administration into the subarachnoid space can reduce the degeneration of spinal nerve fibers, resulting in the existence of a very small number of corticospinal tract fibers in the spinal cord injury area. , may be beneficial to the repair of spinal cord injury [10]. Research in recent years has shown that cyclic adenosine monophosphate can mimic the effects of nerve growth factor in promoting nerve growth, survival and differentiation. By injecting cyclic adenosine monophosphate into the target muscle, part of the cyclic adenosine monophosphate is absorbed into the blood and acts on spinal cord neurons. The other part may increase the concentration of cyclic adenosine monophosphate in the muscle cells and then pass through the neuromuscular junction to reach the nerve injury area and exert its effects. Nerve regeneration. In addition, the injection of cyclic adenosine monophosphate into the target muscle can exert a local nutritional effect on the target muscle, effectively prevent the atrophy of the target muscle, maintain the activity of the neuromotor end plate, and facilitate functional recovery after nerve regeneration. However, the mechanism of action of cyclic adenosine monophosphate on peripheral nerve regeneration is still unclear and needs further study.
- Treatment of liver and gallbladder diseases
The prominent clinical manifestation of chronic cholestatic hepatitis is intrahepatic cholestasis, and its jaundice lasts for a long time and is difficult to treat. Subsidence often leads to further deterioration of liver function. Clinical use of cAMP combined with FDP to treat chronic cholestatic hepatitis has found that while promoting the recovery of liver function, it can significantly promote the regression of jaundice and eliminate or improve intrahepatic cholestasis. Its mechanism of action may be: using cAMP to increase�The content of cAMP in plasma and hepatocytes can thereby increase bile flow and increase bile excretion; FDP can promote the synthesis of ATP in hepatocytes, improve hepatocyte hypoxia and restore their functions, and can also promote potassium ions and sodium ions in hepatocytes. The exchange of ions can significantly improve the retention of intracellular sodium ions, thereby promoting the subsidence of hepatocyte edema, and the phenomenon of bile canaliculi compression and cholestasis is also improved, so that bile flows smoothly and jaundice subsides. Since the two drugs have different anti-jaundice mechanisms, the combined effect is good and there are no adverse reactions.
- Treat respiratory diseases
Bronchial asthma attacks are mainly caused by spasm of bronchial smooth muscle. There are many causes of bronchial asthma, but it is generally believed that Related to immunological abnormalities and autonomic nervous system dysfunction. It is currently believed that these two types of causes are related to the reduction of cAMP/cGMP ratio at the molecular level. The intracellular cAMP/cGMP ratio has a direct effect on the tension of bronchial smooth muscle. Any medium or substance that can increase the cAMP/cGMP ratio can cause bronchial relaxation, and vice versa can cause it to contract. Clinical observation shows that cAMP can improve myocardial hypoxia, expand coronary arteries, enhance myocardial contractility, and increase cardiac blood output. It has no obvious adverse reactions and is suitable for children with heart failure. On the basis of conventional treatment, the clinical application of cyclic adenosine monophosphate has shown positive inotropic, vasodilatory, and antiarrhythmic effects. As the second messenger of life information transmission, cAMP can release Ca2+ from the ATP-Ca2+ complex on the cell membrane to change the function of the cell membrane; it can also cause Ca2+ in the sarcoplasmic reticulum to enter the muscle fiber, thereby enhancing myocardial contractility and increasing cardiac function. discharge, and dilate the coronary arteries. Clinical observations show that exogenous cyclic adenosine monophosphate (cAMP) entering the body can directly or indirectly activate a series of protein kinases, increase the role of phosphorylase, and decompose glycogen to supply energy during hypoxia, thereby promoting oxidation of the respiratory chain. Activation of enzymes improves myocardial hypoxia; inhibits the production of free radicals to prevent ischemia-reperfusion injury; increases the concentration of cAMP in the blood, thereby reducing the inflammatory response after ischemia and improving capillary permeability changes caused by ischemia .
References:
[1] Han Lingzhi, Dai Xuewu. The adjuvant therapeutic effect of cyclophosphate adenosine in the acute phase of chronic congestive heart failure [J]. Primary Medicine Forum, 2005, 9(11): 987-988.
[2] Hui Haosheng, Liang Gaoyan, Wu Keng. Study on the clinical efficacy of cyclophosphate adenosine in the treatment of acute exacerbation of chronic congestive heart failure [J]. Journal of Physician Advanced Education, 2005, 28(4): 32-33.
[3] Lu Yuli, He Mengguo, Ren Nansha, et al. Clinical observation of cyclic adenosine monophosphate injection in the treatment of congestive heart failure [J]. Journal of Cardiovascular Rehabilitation, 2006, 15(1): 49-50.
[4] Tao Xing, Tian Ming, Huai Qingyuan. Effect of injection of cyclic adenosine monophosphate on perioperative hemodynamics in patients undergoing coronary artery bypass surgery [J]. Chinese Medical Journal, 2006, 86(12):859 -861.
